Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent clinical experiences with 34 Z-E patients indicates that the clinical features and course of the syndrome is less dramatic than described originally. Eighty-five per cent of the patients presented stories of abdominal complaints lasting more than five years and resembling the complaints presented by duodenal ulcer patients (DU). Ulcers were present in 91 per cent of the patients. Fifty-one per cent had either ectopic or multiple ulcers. One third had a single duodenal ulcer resembling an ordinary ulcer. No patients died from complications to the ulcer diathesis. Marked hypersecretion of acid and gastrin was present in the ZE group (BAO:33.7 +/- 7.4; PAO:62.8 +/- 6.1 meq H+/h; gastrin: 5094 pmol/l), but because of great individual variation in the ZE, some overlapping with the acid and gastrin measurements of the DU was seen. The diagnostic value of provocative tests using secretin, calcium, glucagon and food stimulations demonstrated a considerable overlapping between the two groups, indicating that these tests are of little clinical value. Tumours were found in half the patients, revealing malignancy in ten. The ZE can be diagnosed in most cases by combining symptomatology, with measurements of acid and gastrin.
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PMID:The clinical diagnosis of the Zollinger-Ellison syndrome. 29 36

The inhibitory effects of intravenous infusions of secretin, glucagon and caerulein on the gastric acid response to bombesin were studied in 8 duodenal ulcer patients. Bombesin was found to be a very potent stimulator of gastric acid secretion in patients with duodenal ulcer. There were no significant differences in acid outputs per 15-min period between bombesin infused in a dose of 0.9 microgram/kg/h and pentagastrin infusion administered in a maximal dose, at a rate of 6.0 microgram/kg/h. Secretin (1 U/kg/h), glucagon (30 microgram/kg/h) and caerulein (0.1 microgram/kg/h) produced significant decreases in gastric acid secretion evoked by bombesin given in a dose of 0.9 microgram/kg/h. Percentages of inhibition were 48.6, 45.2 and 35.5, respectively. It is supposed that secretin and glucagon given in pharmacological doses are capable of interfering with the action of gastrin released from antrum by means of bombesin on the parietal cell by noncompetitive kinetics. Caerulein administered in a pharmacological dosis, however, can inhibit the effect of gastrin released by bombesin on the parietal cells by a competitive kinetic.
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PMID:Inhibition of bombesin-stimulated gastric acid secretion by secretin, glucagon and caerulein in patients with duodenal ulcer. 48 52

The blood serum levels of gastrin and insulin and arterial blood levels of glucose were determined immediately before intravenous injection of 1 mg of glucagon, and 10, 20, 40 and 60 minutes later in 12 gastric ulcer patients, 14 duodenal ulcer patients and 12 controls using the radioimmunological and orthotoluidine methods respectively. Following glucagon administration the gastrin levels dropped in the controls and the gastrin patients, and increased in the duodenal patients by an average of 30%. Insulin levels increased in all three groups, but the increase was statistically significant in the two patients groups. Glucose levels in the blood also increased with no significant differences between the groups. It is suggested that the different effect of glucagon on gastrin levels may be due to gastrin-insulin interaction; the levels of the two hormones in the blood of duodenal patients were higher than in the other two groups studied.
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PMID:The effect of glucagon on the blood levels of gastrin, insulin and glucose in patients with gastric and duodenal ulcers. 52 17

In 10 duodenal ulcer patients gastric acid secretion was stimulated by intravenous infusion of 1.5 microgram pentagastrin per kilogram hour. When acid secretion had reached a plateau, glucagon in a dose of 30 microgram per kilogram hour, secretin in a dose of 1 IU per kilogram hour or caerulein in a dose of 0.1 microgram per kilogram hour were infused into a separate vein for one hour during the intravenous infusion of pentagastrin. Using these doses, each drug produced about 30 per cent inhibition given separately. The highest degree of inhibition was obtained by the combination of glucagon and secretin. The inhibition reached the sum of the inhibitions after glucagon and secretin administered separately. Caerulein added to glucagon or secretin could slightly increase the inhibitory effect of these drugs given separately. Caerulein, however, failed to increase inhibition when glucagon and secretin were infused simultaneously.
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PMID:Inhibitory effect of glucagon, secretin and caerulein on gastric acid secretion stimulated by pentagastrin in patients with duodenal ulcer. 72 19

The effect of glucagon on gastric acid and pepsin secretion, basal or stimulated by a meal, pentagastrin and histamine, was studied in duodenal ulcer patients. Intravenous glucagon infused in graded doses ranging from 6.2 to 50 mug per kg-hr produced a dose-related inhibition of pentagastrin-induced acid secretion reaching about 40% of the control level at the dose of 50 mug per kg-hr. Acid inhibition was paralleled by a decrease in the pepsin output and serum calcium level and was accompanied by a rise in the blood glucose concentration. Glucagon used in a standard dose of 25 mug per kg-hr produced about 50% inhibition of acid secretion induced by a meal (measured by intragastric titration) accompanied by a significant decrease in the serum gastrin level measured by radioimmunoassay. Histamine-induced secretion was only slightly inhibited by glucagon, and the degree of inhibition for acid (25%) and pepsin (20%) secretion was statistically insignificant.
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PMID:Effect of glucagon on meal-induced gastric secretion in man. 108 77

In healthy controls (n = 7), patients with duodenal ulcer (n = 7), primary hyperparathyroidism (n = 7), and 1 case of excluded gastric antrum the effects of intravenous secretin ("Karolinska"; 3 U/kg/h for 90 min) upon serum calcium fractions, total protein, and the integrated response of gastrin and glucagon were investigated. In all groups total calcium, total protein, and protein-bound calcium fraction rose significantly but the inonized calcium fraction remained stable. Since serum concentration of gastrin and glucagon could not be altered in any of the groups a direct interference of these hormones with calcium homeostasis during secretin infusion can be ruled out. Hyperparathyroid patients had higher baseline glucagon values (209 +/- 30 pg/ml) than normals (127 +/- 6 pg/ml) and ulcer patients (138 +/- 11 pg/ml) and maintained a higher hormone output throughout the experiment. Together with data on the patient with excluded antral parts it is concluded that the hypercalcemic effect of secretin is not mediated by calcium-regulating hormones but must be of an unspecific nature.
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PMID:Studies on the calcemic effect of intravenous secretin in humans. 122 May 13

A total of 24 patients with endocrine neoplasms of the pancreas were clinicopathologically and immunohistochemically studied. They consisted of 18 patients with adenoma and 6 with carcinoma. Of the 24 patients, 13 developed attacks of hypoglycemia due to hyperinsulinemia, and 1 developed an uncontrollable duodenal ulcer caused by the hypersecretion of gastrin, however, the remaining 10 were asymptomatic. No prediction could be made as to the site of origin of the tumors. A clear difference was seen between adenoma and carcinoma in the size of the mass, the mean greatest diameter of the 18 adenoma cases being 1.7 cm, while that of the 6 carcinoma cases was 7.3 cm. One of the 13 insulinomas and a gastrinoma was malignant, while all 24 tumors were positive for neuron-specific enolase. The 13 insulinomas were diffusely positive for insulin and 5 were also shown to be focally immunoreactive for gastrin, with 3 also being immunoreactive for somatostatin and 2 for pancreatic polypeptide. The gastrinoma showed immunoreactivity for somatostatin, insulin, pancreatic polypeptide, and glucagon in addition to a positivity to gastrin. The above findings thus indicate the multiple hormone synthesis of endocrine neoplasms of the pancreas.
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PMID:Endocrine neoplasms of the pancreas: a clinicopathologic study of 24 cases and immunohistochemical remarks. 139 40

The response of serum gastrin, insulin and glucagon to administration of sodium bicarbonate (SB) followed by cimetidine was studied in 35 duodenal ulcer patients. Relevant measurements were made using radioimmunoassay kits "Diagnostic" (USA) and "Oris" (France). It was established that SB administration induced a significant rise in gastrin levels while those of insulin, glucagon and gastrin lowered significantly following cimetidine treatment (gastrin levels progressed to baselines). This marked effect of cimetidine on the gut hormone production is not always due to its adverse action being rather of compensatory nature and directed at enhancement of cytoprotection and normalization of gastric secretion.
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PMID:[Gastrin, insulin and glucagon secretion after cimetidine and sodium hydrocarbonate intake in patients with duodenal ulcer]. 164 49

Blood serum insulin, glucagon, pepsinogen, trypsin was studied by radioimmunological methods in 95 patients with ulcer disease. Fasting values and values 1 and 2 hours after a standard breakfast (1212 kcal) were evaluated. It was established that all patients showed a statistically valid increase of the basal level of glucagon while patients with gastric ulcer showed an increase of the basal insulin level. Use of a test breakfast showed reserve and compensatory capacities of the hormonal pancreatic function. Patients with gastric and duodenal ulcer revealed an increase of the pepsinogen level under conditions of basal secretion and after a test breakfast.
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PMID:[Pancreatic hormonal function and proteolytic activity in peptic ulcer]. 208 6

The aims of the present study were to determine in 14 healthy subjects and 14 duodenal ulcer patients the reproducibility of the acid secretory response to a modified sham-feeding test and the effect on this response of intrajejunal hypertonic glucose instillation, in order to evaluate the possibility of the existence of a defective inhibition of the cephalic phase of gastric acid secretion in duodenal ulcer disease. The reproducibility of the acid secretory response to a modified sham-feeding test was demonstrated in both groups in two consecutive tests. The hypertonic glucose instillation produced a significant inhibition of the acid secretory response to modified sham feeding only in the healthy subjects, suggesting that duodenal ulcer patients may have a defective mechanism of acid inhibition during vagal stimulation by modified sham feeding. Non-significant changes were observed in plasma gastrin and pancreatic glucagon levels.
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PMID:Influence of jejunal hypertonic glucose infusion on sham-feeding-stimulated gastric acid secretion: evidence of a defective mechanism in duodenal ulcer patients. 232 Sep 45


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